TECRL mutations impair SR calcium loading and prolong action potential repolarization, presenting a mixed phenotype of LQTS and CPVT [132]; PPP1R3A, a regulatory subunit of PP1, anchors to RyR2 and PLN, modulating their phosphorylation state and protecting against aberrant calcium release and atrial structural instability [133]; SCN1A mutations increase sodium current and spontaneous beating in iPSC-derived cardiomyocytes, potentially linking epilepsy-associated genes to cardiac excitability [134]. This evidence concerns the gene SCN1A and familial long QT syndrome.